Cell Signaling Responses in Concurrent Training

Cell Signaling Responses in Concurrent Training

Endurance Training

  • High volume of repetitive, lower intensity contractions.
  • Increases AMP to ATP ratio and calcium release.
  • Activates the AMPK (5' adenosine monophosphate-activated protein kinase) pathway.
    • AMPK is a fuel sensor in the cell.
    • Improves glucose uptake.
    • Increases mitochondria density.
    • Increases fat metabolism.
    • Decreases muscle protein synthesis.

Weight Training

  • High intensity, low volume contractions.
  • Profound effects on insulin and insulin-like growth factor.
  • Activates the AKT (protein kinase B) pathway in skeletal muscle.
    • Increases protein synthesis.
    • Increases cell growth.
    • Increases glucose transport.
    • Decreases protein degradation.

Competing Interests in Concurrent Training

  • Endurance training stimulates the AMPK pathway for mitochondrial biogenesis.
  • Weight training stimulates the AKT pathway for muscle protein synthesis.
  • Concurrent training affects physiological processes.

Pathway 1: Cycling Exercise

  • Large amount of contractions and calcium release.
  • Acts on CAMK (calmodulin-dependent kinase).
  • CAMK phosphorylates EEF2, blocking the ribosome and mRNA translation.

Pathway 2: Resistance Training

  • Increases activity of S6K.
  • S6K blocks EEF2K.
  • This then blocks the phosphorylation of EEF2.
  • Allows mRNA translation to occur.

FOXO1 Proteins and Transcription Activation

  • Cycling pathway: FOXO1 activates PGC-1alpha, resulting in mitochondrial biogenesis.
  • Resistance training pathway: AKT stimulation phosphorylates FOXO1 proteins, leading to the MAFBX pathway and decreased protein degradation.

Resistance Training and mTOR

  • Activates P13K and the AKT pathway.
  • AKT upregulates mTOR (mammalian target of rapamycin), promoting muscle protein synthesis.
  • mTOR acts on the 4E-BP1 pathway to block EIF4E.
  • mTORmTOR is a crucial switch for muscle protein synthesis and muscle hypertrophy.
  • Anything with an arrow means it's a positive stimulator; anything with a blunt line blocks the next step.

Endurance Training Pathways

  • Affects the P38 MAPK pathway.
  • Increasing calcium increases activity of calcium MK.
  • Activates the AMPK pathway.
  • All three stimulate and improve mitochondrial biogenesis.
  • AMPK activates TORC signaling (TSC1 and TSC2).
  • Activation of TORC signaling 1 and 2 blocks mTOR activity.
  • Blocking mTOR inhibits muscle protein synthesis.

Impact of Glycogen Levels

  • Decreases in glycogen and increases in AMP stimulate AMPK through phosphorylation.
  • TORC signaling two becomes phosphorylated, blocking mTOR actions.
  • AMPK pathway leads to increased mitochondrial biogenesis and improved aerobic capacity.
  • Decrease in glycogen stimulates AMPK activity.
  • If resistance training is performed in a glycogen-depleted state, AMPK activity is upregulated, which is detrimental.

Exercise Order

  • Resistance exercise performed before cycling leads to upregulation of AKT compared to cycling performed alone.
  • TORC signaling two is greater when cycling is performed.
  • mTOR is slightly higher when resistance exercise is performed before cycling exercise.
  • AMPK activity increases when cycling is performed compared to when resistance exercise is performed.

Coffey et al. (2009) Study

  • Examined IGF and mRNA expressions (MyoD and MRF).
  • MRF protein expression was higher when resistance exercise was performed before cycling exercise.
  • Individual changes are important to consider, not just group bar graphs.
  • Bar graphs can be misleading; individual data shows varying responses.
  • Consistent directional changes across subjects indicate a more robust finding.

mRNA Abundance and Myogenic Responses

  • Endurance training increases MyoD, Myogenin, MAFBX, and myostatin, indicating a blunted muscle hypertrophy response.
  • Myostatin is a strong regulator of hypertrophy; increased activity impedes hypertrophy.
  • Strength training shows a non-significant increase in PGC1 alpha.

Fife et al. Study

  • Endurance exercise influences CAMK2, AMPK, SIRT1, and HIF-1alpha (hypoxic-inducible factor 1 alpha).
  • HIF-1alpha stimulates REDD1 and activates TORC signaling two.
  • TORC signaling two blocks the mTOR pathway, which is detrimental for muscle hypertrophy.
  • AMPK can block mTOR through TORC signaling two or by acting directly on raptor.
  • Actions decrease elongation and translation initiation, reducing rates of protein synthesis.
  • AMPK influences ubiquitin proteasome system and autophagy lysosomal system, increasing rates of protein breakdown.
  • Overall, leads to a decrease in muscle fiber hypertrophy.

p53 and Zestrin

  • Aging, fasting, endurance training, and redox reactions increase stress, activating p53 and influencing Zestrin.
  • These steps downregulate mTOR muscle protein synthesis.
  • Proper nutrition and feeding, especially with high amounts of leucine, can block Zestrin activity and negative effects.
  • Stress from endurance exercise, fasting, shifts in redox state, or aging can increase p53, leading to decreased polymerase one activity and reduced production of 45S pre-ribosomal RNA.
  • Stress can influence p53 and be detrimental for muscle protein synthesis.

Practical Considerations for Concurrent Training (Fife et al.)

  • Aerobic training prior to resistance exercise (in close proximity), increased aerobic exercise intensity and volume can lead to substrate depletions and increased residual fatigue.
  • Residual fatigue results in decreased force production and decreased type II fiber activation, compromising the resistance exercise training stimulus.
  • Substrate depletion (glycogen depletion and increased amino acid oxidation) decreases the anabolic response to resistance exercise.
  • Decreased mTOR activation and decreased rates of protein synthesis.
  • Increased catabolic response and increased rates of protein breakdown.
  • Ultimately leads to a decrease in muscle fiber hypertrophy.

Conclusions

  • Cell signaling evidence indicates that resistance and endurance training result in different cellular signaling responses.
  • Concurrent training can create an interference effect, where strength development is not optimized.
  • Training status can impact cell signaling responses.
  • More research is needed to explore cell signaling responses in periodized training models and their effects on performance and adaptations.
  • Many studies use resistance training models with repetitions performed to fatigue or repetition maximum across the training period, which may not be ideal.